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Plasma and cerebrospinal fluid tau and neurofilament concentrations in rapidly progressive neurological syndromes: a neuropathology-based cohort

Artikel i vetenskaplig tidskrift
Författare G. G. Kovacs
Ulf Andreasson
V. Liman
G. Regelsberger
M. I. Lutz
K. Danics
E. Keller
Henrik Zetterberg
Kaj Blennow
Publicerad i European Journal of Neurology
Volym 24
Nummer/häfte 11
Sidor 1326-+
ISSN 1351-5101
Publiceringsår 2017
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 1326-+
Språk en
Länkar dx.doi.org/10.1111/ene.13389
Ämnesord Alzheimer disease, Creutzfeldt-Jakob disease, neurodegeneration, neurofilament light chain, rapidly, creutzfeldt-jakob-disease, protease-sensitive prionopathy, traumatic, brain-injury, alzheimers-disease, neurodegenerative diseases, neurofibrillary pathology, frontotemporal dementia, csf biomarkers, prion protein, light protein, Neurosciences & Neurology
Ämneskategorier Neurovetenskap

Sammanfattning

Background and purposeCerebrospinal fluid (CSF) tau and neurofilament light chain (NF-L) proteins have proved to be reliable biomarkers for neuronal damage; however, there is a strong need for blood-based tests. MethodsThe present study included 132 autopsy cases with rapidly progressive neurological syndromes, including Alzheimer disease (AD) (21), sporadic (65) and genetic (21) Creutzfeldt-Jakob disease (CJD), 25 cases with vascular, neoplastic and inflammatory alterations, and additionally 18 healthy control individuals. CSF tau and NF-L concentrations were measured by enzyme-linked immunosorbent assay. Plasma tau and NF-L concentrations were measured using ultra-sensitive single molecule array technology. ResultsPlasma and CSF tau (R = 0.59, P < 0.001) and NF-L (R = 0.69, P < 0.001) levels correlated significantly (Spearman test). Plasma tau and NF-L levels were significantly higher in all disease groups compared to healthy controls (P < 0.001). Receiver operating characteristic curves were used and area under the curve values for comparisons with controls were 0.82 (AD), 0.94 (sporadic CJD), 0.92 (genetic CJD) and 0.83 (other neurological disorders) for plasma tau and 0.99, 0.99, 1.00 and 0.96 for plasma NF-L, respectively. Molecular subtyping of sporadic CJD showed a strong effect (linear logistic regression) on plasma tau (P < 0.001) but not NF-L levels (P = 0.19). ConclusionPlasma tau and NF-L concentrations are strongly increased in CJD and show similar diagnostic performance to the corresponding CSF measure. Molecular subtypes of sporadic CJD show different levels of plasma tau. Although not disease-specific, these findings support the use of plasma tau and NF-L as tools to identify, or to rule out, neurodegeneration.

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